Objective To observe the changes on the neurogenic inflammation-related factors in the dura mater of the rat model of migraine and investigate the possible mechanism of the pain of migraine.Methods SD rats were randomly divided into stimulation group ( n = 32 ) and sham group ( n = 32 ).Unilateral trigeminal ganglion was stimulated to induce migraine for rats in the stimulation group. Rats in the sham group were subjected to sham surgery. The levels of calcitonin gene-related peptide (CGRP) in the blood of jugular vein in the stimulation side were measured by radioimmunoassay. The levels of histamine in peripheral blood and prostaglandin E2 (PGE2 ) in the dura mater were determined by enzyme-linked immunosorbent assay (ELISA). The number of mast cells and percentage of their degranulation in the dura mater were determined under a microscope after toluidine blue staining. Cyclooxygenase 2 (COX-2)expression in the dura mater was evaluated by immunohistochemical staining and western blot analysis. Results In the stimulation group, the level of CGRP in the ipsilateral jugular vein was (82. 84 ± 16. 24)pg/ml and in the sham group was (59. 20 ±11.66) pg/ml (t = -3.34, P ＜ 0. 05 ). The level of histamine in the ipsilateral jugular vein was ( 11.59 ± 1.20) ng/ml and in the sham group was (9. 87 ±0. 88) ng/ml (t = - 3. 27, P ＜ 0. 05). The number of mast cells in the dura mater decreased from 15.46 ± 2. 40 in the stimulation group to 11.63 ± 1.67 in the sham group ( t = 3.71, P ＜ 0. 05 ). Degranulation of mast cells in the dura mater significantly increased from 14. 09% ±4. 53% in the sham group to 29. 10% ±9. 39% in the stimulation group (t = - 4. 07, P ＜ 0. 05 ). The level of PGE2 in the stimulation group was ( 382. 30 ±20. 90) pg/ml and in the sham group was (80. 70 ± 10. 60) pg/ml (t = - 16. 674, P ＜0. 05). The number of COX-2 positive cells significantly increased from 42. 00 ± 18.40 in the sham group to 139.00 ±20. 50 in the stimulation group (t = -7. 994, P ＜0. 05). Also the COX-2 protein level was elevated from 19. 50 ±9. 20 in the sham group to 359. 20 ±21.90 in the stimulation group (t = -5. 190, P ＜0. 05). Conclusions Electrical stimulation on the unilateral trigeminal ganglion induces neurogenic inflammation in the dura mater. Changes on the neurogenic inflammation-related factors are probably the essential pathophysiological mechanism underlying the pain in migraine.

Objective To explore the effects of astrocytes in cervical spinal cord posterior horn on allodynia in rat models of migraine.Methods Fifty-four male SD rats were randomly divided into 9 groups (each group n =6): blank group,sham surgery group,new inflammatory soup 3 d group (IS 3 d group),new inflammatory soup 7 d group(IS 7 d group),saline group,fluorocitrate (FCA)prevention group,FCA prevention control group,FCA treatment group,FCA treatment control group.Following the IS stimulation in the rat dual matter,Von-Frey hair was used to monitor the pain threshold of periorbital skin.Immunofluorescence technique was used to observe the expression of specific marker of astrocyte,glial fibrilary acidic protein (GFAP),and neuron activation marker,C-fos.Results ①Von-Frey hair study showed the thresholds of IS 3 d group and IS 7 d group were significantly decreased compared with the control group(3 d:5.3 ±0.3 vs 6.4 ±0.3,F =40.15;7 d:3.0 ±0.3 vs 6.3 ±0.2,F =382.5,both P ＜0.01).The pain thresholds of FCA prevention group and FCA treatment group both began to significantly increase at the day 4 (FCA prevention:5.5 ± 5.1 vs 5.1 ± 0.2,F =16.00 ;FCA treatment:4.3 ± 0.2 vs 3.0 ± 0.2,F =138.0,both P ＜ 0.01).②GFAP immunofluorescence showed that the mean optical density (A) values of IS 3 d group and IS 7 d group were significantly increased compared with the control group(3 d:24.5 ±4.4 vs 14.8 ± 2.5,F =32.54;7 d:38.9 ± 7.1 vs 14.6 ± 1.8,F =63.56,both P ＜ 0.01).()C-fosimmunofluorescence showed that mean A value of IS 3 d group was significantly increased compared with the control group (20.4 ± 2.3 vs 8.4 ± 1.1,F =129.0,P ＜ 0.01).The difference was not significant between the IS 7 d group and the control group.Conclusions Activated astrocytes contribute to the facial allodynia induced by chronic dural inflammation.Its inhibitor FCA could both prevent and treat the allodynia behaviour.All of these suggest that astrocytes may not only contribute to the initiation of mechanical allodynia but also the maintenance.

ObjectiveTo determine the prevalence of avian influenza viruses in the external environment of poultry in Anqing City， Anhui Province， and provide scientific evidence for prevention and control of animal-derived influenza in humans. MethodsA total of 28 farmers’ markets/farms in 10 counties （cities， districts） of Anqing City， Anhui Province， were selected as surveillance sites by simple random sampling strategy. Poultry faeces and other related samples were collected for 6 consecutive weeks. Real-time fluorescence quantitative PCR was used to examine the nucleic acids of influenza A virus. Subtypes H5， H7， and H9 of avian influenza virus were further tested in the positive samples. ResultsA total of 426 specimens were collected， among which 113 tested positive with a positive rate of 26.53%. Among the positive specimens， 104 were determined to be subtype H9， accounting for 92.04%. It did not significantly differ in the positive rate between the main and non-main urban areas （χ²<0.01， P>0.05） or among the specimens collected in different weeks （χ²=7.57， P>0.05）. However， it significantly differed in the positive rate among the specimens collected in the third week and other weeks （χ²=6.89， P<0.05）. Furthermore， among the different sampling sites， farms had the highest positive rate of 46.67%. Among the specimens from different sources， the surface-coated specimens from poultry cages had the highest positive rate of 34.78%. ConclusionAvian influenza viruses are prevalent in the external environment of poultry in Anqing City. It warrants strengthening the surveillance and risk assessment to reduce the virus transmission in the external environment and risk of human infection with animal-derived influenza.